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氯氨酮减轻高血糖大鼠脑缺血所致的神经元凋亡
http://www.100md.com 《第四军医大学学报》 2006年第18期
高血糖症;脑缺血;氯胺酮;细胞外信号调节MAP激酶类;细胞凋亡;免疫组织化学;免疫印迹法,,高血糖症;脑缺血;氯胺酮;细胞外信号调节MAP激酶类;细胞凋亡;免疫组织化学;免疫印迹法,氯氨酮减轻高
     Role of ketamine in decreasing neuronal apoptosis caused by brain ischemia in rats with hyperglycemia

    ZHANG JianZhong, JING Li, GUO FengYing, MA Yi, WANG YiLi

    Institute of Immunopathology, School of Life Science & Technology, Xian Jiaotong University, Xian 710061, China, Department of Pathology,Ningxia Medical College, Yinchuan 750004, China

    【Abstract】 AIM: To investigate the mechanism by which ketamine reduces the aggravation of hyperglycemiainduced cerebral ischemic lesion. METHODS: Rats with normoglycemia, hyperglycemia, or hyperglycemia pretreated with ketamine injection were subjected to 15 min of global brain ischemia, and then reperfused for 0.5, 1, and 3 h, respectively. Phosphorylation of extracellular signalregulated kinase (ERK)1/2 was assessed by immunohistochemistry and Western blot analysis. Meanwhile, the neuronal apoptosis was observed by TdTmediated dUTP nickend labeling (TUNEL). RESULTS: The phosphorylation of ERK1/2 in the regions of cingulum cortex, hippocampus CA1 and CA3, were significantly increased in ischemic rats with normoglycemia reperfused for 0.5 h. Compared to the normoglycemic group, the phosphorylation of ERK1/2 in the regions of cingulum cortex and hippocampus CA3 were also significantly increased in hyperglycemic group reperfused for 0.5 h, which lasted to 3 h of reperfusion. However, this augmentation of phosphorylation was depressed by ketamine administration in hyperglycemic rats. The extent of ERK1/2 phosphorylation was consistent with the ischemic brain lesions, observed by histology as neuronal apoptosis. CONCLUSION: Hyperglycemia may increase the ischemic insult via the modulation of ERK1/2 signal transduction pathways. Ketamine improves the aggravation of hyperglycemiainduced cerebral ischemic lesion. This is probably mediated by inhibition of NMDAmediated calcium influx, and hyperglycemiainduced phosphorylation of ERK1/2. ......

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